Current clinical and pathogenetic understanding of beta2-m amyloidosis in long-term haemodialysis patients.

As the number of patients undergoing long-term haemodialysis continues to grow, beta2-microglubulin (beta2-m) amyloidosis is emerging as an increasingly common complication. The frequency of beta2-m amyloid-related osteoarthropathy in haemodialysis patients rises steadily with length of survival. We confirmed that the prevalence of carpal tunnel syndrome increases with years of dialysis. Up to 50% of patients had developed this complication after 20 years were affected and the percentage was even higher after 25 years. Although retention of beta2-m is a necessary requirement for onset of amyloidosis, it is probably not sufficient. Using an in vitro model of beta2-m-related amyloid fibril (fAbeta2-m) extension, we demonstrated that various amyloid-associated molecules, such as apolipoprotein (apo) E and proteoglycans, accelerate beta2-m amyloid fibril formation. General categories of therapeutic approaches for amyloidosis include prevention of onset or progression, symptomatic therapy (conservative treatment, orthopedic procedures, and physiotherapy), and renal transplantation. In association of haemodialysis, beta2-m has been removed by high-flux membranes or a beta2-m adsorption column. However, proof is lacking that amyloid deposits are decreased by long-term use of dialysis techniques to eliminate beta2-m. More effective treatment procedures are needed.